Pollution's Cancerous Effects: Understanding The Deadly Link

Air pollution is a complex mixture of tiny solid and liquid particles in the air, including acids, organic chemicals, metals, soil, and dust particles. These particles are emitted from wood stoves, forest fires, vehicles, factories, and power plants. Outdoor air pollution is mostly caused by transport, power generation, industrial or agricultural emissions, and residential heating and cooking.

Research has shown that air pollution is laced with cancer-causing substances. In 2013, the World Health Organization (WHO) concluded that particulate matter in the air causes lung cancer. A study in Hong Kong found that for every 10 micrograms per cubic meter (µg/m3) of increased exposure to PM2.5, the risk of dying from any cancer rose by 22%. The same study also found that the risk of mortality for cancers of the upper digestive tract was 42% higher, and for cancers of the accessory digestive organs, it was 35% higher.

While air pollution has been linked to an increased risk of lung cancer, it is important to note that smoking has a much bigger impact on lung cancer risk. However, air pollution can also cause inflammation in the lungs, which can lead to cancer.

To reduce the risk of cancer from air pollution, individuals can limit their activity when pollution levels are high and avoid exercising along heavily traveled highways. Additionally, not burning wood or trash and reducing vehicle idling can help lower local pollution levels.

Outdoor air pollution

Particulate matter, especially fine particulate matter (PM2.5), has been linked to an increased risk of lung cancer incidence and mortality. Studies have also found associations between outdoor air pollution and an increased risk of other types of cancer, such as bladder and breast cancer, although more research is needed in this area.

The biological mechanisms behind air pollution-related carcinogenesis are not yet fully understood, but it is believed that air pollutants can generate effects along the respiratory tract, leading to inflammation and oxidative stress, which are critical drivers of carcinogenesis.

Indoor air pollution

In addition to cancer, indoor air pollution can lead to stroke, respiratory, and cardiovascular diseases. It can also negatively impact the quality of life of people living with cancer by exacerbating respiratory symptoms, increasing fatigue, reducing physical activity, and worsening treatment side effects.

To reduce the health risks associated with indoor air pollution, it is important to improve air quality by reducing exposure to fine particulate matter. This can be achieved through various measures, such as increasing green spaces, transitioning to cleaner energy sources, and promoting active transportation (walking and cycling).

Particulate matter

Research has linked particulate matter to an increased risk of lung cancer. A study in Hong Kong found that for every 10 micrograms per cubic meter (µg/m3) of increased exposure to PM2.5, the risk of dying from any cancer rose by 22%. Another study by the World Health Organization (WHO) International Agency for Research on Cancer concluded that particulate matter causes lung cancer.

In addition to lung cancer, particulate matter has been associated with other adverse health effects. Short-term exposure to high levels of particulate matter can trigger cardiovascular events, hospital admissions, and even mortality. Long-term exposure can increase the risk of strokes, coronary heart disease, lung cancer, and premature death.

While everyone is at risk from the health impacts of particulate matter, certain individuals are more vulnerable. These include pregnant women, infants, children, the elderly, people with lung or heart disease, people with low socioeconomic status, and current or former smokers.

To protect ourselves from particulate matter, it is recommended to check the air quality index forecast and limit outdoor activities if pollution levels are high. Policymakers also have a role in implementing measures to reduce particulate matter pollution and improve air quality.

Inflammation in the lungs

Air pollution can cause inflammation in the lungs, which can lead to other serious health conditions. Particles of pollution enter the body and the innate immune response kicks in, leading to the production of cytokines and other molecules that produce inflammation to fight off the invader. This inflammation can cause harm, especially when exposures pile on top of each other.

Particles deposited in the respiratory tract in sufficient amounts can induce inflammation, and the extent of pulmonary inflammation depends on the particle dose and composition. Controlled human exposure studies have demonstrated increased markers for pulmonary inflammation following exposure to a variety of different particle types. For example, organic carbon particles and transition metals from combustion sources can elicit a strong inflammatory response.

Airway inflammation increases airway responsiveness to irritants and may reduce lung function by causing bronchoconstriction. At a cellular level, inflammation may damage or kill cells and compromise the integrity of the alveolar-capillary barrier. Repeated exposure to particle pollution aggravates the initial injury and promotes chronic inflammation with cellular proliferation and extracellular matrix reorganization.

The most damaging particles are the smaller 'fine' particles that cannot be seen, known as PM10 and PM2.5, and the ultrafine particles. PM10 particles can reach your airways, while PM2.5 particles can reach the breathing sacs in your lungs. Ultrafine particles can cross into your bloodstream, and these particles can also carry toxic chemicals that are linked to cancer.

DNA damage

Pollutants can cause cancer by damaging DNA. DNA damage can occur through exogenous and endogenous processes, and can be caused by both chemical and physical agents.

Types of DNA damage

Carcinogens may be categorised as either activation-dependent or activation-independent. Activation-independent carcinogens, also known as direct-acting carcinogens, can interact directly with DNA and other cellular components due to their electrophilic groups. Direct-acting carcinogens include nitrosamines, ultraviolet (UV), ionising radiation and alkylating agents.

Activation-dependent carcinogens, also known as indirect-acting carcinogens, are relatively unreactive parent compounds that require bioactivation in host cells to transform them into carcinogenic metabolites or reactive intermediates that are capable of exerting genotoxic effects. These include polycyclic aromatic hydrocarbons (PAHs), heterocyclic aromatic amines (HAAs), N-nitrosamines, mycotoxins and aristolochic acid (AA).

Types of DNA damage caused by carcinogens

Carcinogens can cause DNA damage through a variety of mechanisms, including:

• Covalent binding of carcinogen with DNA
• DNA double-strand breaks (DSBs) formed as a result of ionising radiation (IR)-induced free radical generation
• Oxidative-induced lesions
• DNA–DNA or DNA–protein cross-links

Human studies of cancers associated with carcinogen-induced DNA damage

There are many human studies that have found an association between environmental and/or dietary exposure to carcinogens and the development of cancer. For example, exposure to carcinogens in tobacco smoke is a prime example of a well-established link between carcinogen-DNA damage and lung cancer.

DNA repair mechanisms

DNA repair mechanisms play an essential role in correcting DNA lesions that occur from DNA-damaging agents or carcinogens, thus maintaining genomic stability. These include base excision repair (BER), nucleotide excision repair (NER), non-homologous end joining (NHEJ) and homologous recombination (HR).

Cancer chemotherapy and radiotherapy are designed to cause apoptosis in cancer cells by inducing catastrophic DNA damage such as DSBs. Traditional therapeutic strategies have been developed based on DNA damage response properties of cancer cells that often have specific abnormalities in the pathway.

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